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Truncated BID (tBID), a proapoptotic BCL2 family protein, induces BAK/BAX-dependent release of cytochrome c and other mitochondrial intermembrane proteins to the cytosol to induce apoptosis. The voltage-dependent anion channels (VDACs) are the primary gates for solutes across the outer mitochondrial membrane (OMM); however, their role in apoptotic OMM permeabilization remains controversial. Here, we report that VDAC2(-/-) (V2(-/-)) mouse embryonic fibroblasts (MEFs) are virtually insensitive to tBID-induced OMM permeabilization and apoptosis, whereas VDAC1(-/-), VDAC3(-/-) and VDAC1(-/-)/VDAC3(-/-) MEFs respond normally to tBID. V2(-/-) MEFs regain tBID sensitivity after VDAC2 expression. Furthermore, V2(-/-) MEFs are deficient in mitochondrial BAK despite normal tBID-mitochondrial binding and BAX/BAK expression. tBID sensitivity of BAK(-/-) MEFs is also reduced, although not to the same extent as V2(-/-) MEFs, which might result from their strong overexpression of BAX. Indeed, addition of recombinant BAX also sensitized V2(-/-) MEFs to tBID. Thus, VDAC2 acts as a crucial component in mitochondrial apoptosis by allowing the mitochondrial recruitment of BAK, thereby controlling tBID-induced OMM permeabilization and cell death.

Titel:	VDAC2 is required for truncated BID-induced mitochondrial apoptosis by recruiting BAK to the mitochondria.
Autor/in / Beteiligte Person:	Roy, SS ; Ehrlich, AM ; Craigen, WJ ; Hajnóczky, G
Link:	Full Text Finder (Volltext)
Zeitschrift:	EMBO reports, Jg. 10 (2009-12-01), Heft 12, S. 1341-7
Veröffentlichung:	2024- : [London] : Nature Publishing Group ; <i>Original Publication</i>: Oxford, UK : Published for EMBO by Oxford University Press, 2000-, 2009
Medientyp:	academicJournal
ISSN:	1469-3178 (electronic)
DOI:	10.1038/embor.2009.219
Schlagwort:	Animals BH3 Interacting Domain Death Agonist Protein genetics Cells, Cultured Drug Resistance drug effects Drug Resistance genetics Embryo, Mammalian Fibroblasts drug effects Fibroblasts metabolism Gene Deletion Gene Knockdown Techniques Mice Mitochondria metabolism Mitochondrial Membranes drug effects Mitochondrial Membranes metabolism Permeability drug effects Protein Transport drug effects Recombinant Proteins pharmacology Voltage-Dependent Anion Channel 2 genetics bcl-2-Associated X Protein genetics bcl-2-Associated X Protein metabolism bcl-2-Associated X Protein physiology Apoptosis drug effects BH3 Interacting Domain Death Agonist Protein pharmacology Mitochondria drug effects Voltage-Dependent Anion Channel 2 physiology bcl-2 Homologous Antagonist-Killer Protein metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural Language: English [EMBO Rep] 2009 Dec; Vol. 10 (12), pp. 1341-7. <i>Date of Electronic Publication: </i>2009 Oct 09. MeSH Terms: Apoptosis / drug effects ; BH3 Interacting Domain Death Agonist Protein / pharmacology ; Mitochondria / drug effects ; Voltage-Dependent Anion Channel 2 / physiology ; bcl-2 Homologous Antagonist-Killer Protein / *metabolism ; Animals ; BH3 Interacting Domain Death Agonist Protein / genetics ; Cells, Cultured ; Drug Resistance / drug effects ; Drug Resistance / genetics ; Embryo, Mammalian ; Fibroblasts / drug effects ; Fibroblasts / metabolism ; Gene Deletion ; Gene Knockdown Techniques ; Mice ; Mitochondria / metabolism ; Mitochondrial Membranes / drug effects ; Mitochondrial Membranes / metabolism ; Permeability / drug effects ; Protein Transport / drug effects ; Recombinant Proteins / pharmacology ; Voltage-Dependent Anion Channel 2 / genetics ; bcl-2-Associated X Protein / genetics ; bcl-2-Associated X Protein / metabolism ; bcl-2-Associated X Protein / physiology Comments: Comment in: EMBO Rep. 2009 Dec;10(12):1311-3. (PMID: 19949413) References: J Biol Chem. 2002 Mar 1;277(9):7610-8. (PMID: 11751859) ; J Cell Biol. 2001 Dec 10;155(6):1003-15. (PMID: 11739410) ; Nature. 1999 Aug 26;400(6747):886-91. (PMID: 10476969) ; Nature. 1999 Jun 3;399(6735):483-7. (PMID: 10365962) ; Science. 2007 Feb 9;315(5813):856-9. (PMID: 17289999) ; J Biol Chem. 2008 May 9;283(19):13482-90. (PMID: 18308720) ; Cell. 2002 Nov 1;111(3):331-42. (PMID: 12419244) ; Science. 2003 Jul 25;301(5632):513-7. (PMID: 12881569) ; Gene. 2006 Mar 15;369:7-19. (PMID: 16446060) ; Nat Cell Biol. 2007 May;9(5):550-5. (PMID: 17417626) ; EMBO J. 1999 May 4;18(9):2330-41. (PMID: 10228148) ; Mol Cell Biol. 2007 Jan;27(2):541-53. (PMID: 17101783) ; Biochim Biophys Acta. 1999 Oct 13;1452(1):68-78. (PMID: 10525161) ; Mol Cell. 1999 Feb;3(2):159-67. (PMID: 10078199) ; EMBO J. 2006 Dec 13;25(24):5635-47. (PMID: 17110923) ; Science. 2001 Apr 27;292(5517):727-30. (PMID: 11326099) ; Cancer Cell. 2002 Sep;2(3):183-92. (PMID: 12242151) ; J Biol Chem. 2002 Feb 15;277(7):5651-9. (PMID: 11741882) ; J Cell Biol. 2008 Nov 17;183(4):681-96. (PMID: 19001123) ; Mol Cell Biochem. 2004 Jan-Feb;256-257(1-2):107-15. (PMID: 14977174) ; J Biol Chem. 2003 Mar 21;278(12):10707-15. (PMID: 12519725) ; J Bioenerg Biomembr. 2008 Jun;40(3):207-12. (PMID: 18622693) ; J Cell Biol. 1999 Mar 8;144(5):891-901. (PMID: 10085289) ; Oncogene. 2008 Jul 10;27(30):4221-32. (PMID: 18362892) ; Mol Cell. 2009 Feb 13;33(3):377-88. (PMID: 19217411) Grant Information: R01 GM059419 United States GM NIGMS NIH HHS; GM59419 United States GM NIGMS NIH HHS Substance Nomenclature: 0 (BH3 Interacting Domain Death Agonist Protein) ; 0 (Bak1 protein, mouse) ; 0 (Bid protein, mouse) ; 0 (Recombinant Proteins) ; 0 (Vdac2 protein, mouse) ; 0 (Voltage-Dependent Anion Channel 2) ; 0 (bcl-2 Homologous Antagonist-Killer Protein) ; 0 (bcl-2-Associated X Protein) Entry Date(s): Date Created: 20091013 Date Completed: 20100330 Latest Revision: 20211020 Update Code: 20231215 PubMed Central ID: PMC2799216

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VDAC2 is required for truncated BID-induced mitochondrial apoptosis by recruiting BAK to the mitochondria.